6533b7cefe1ef96bd1256eee

RESEARCH PRODUCT

Opioid Inhibition of Oxytocin Release, but not Autoinhibition of Dopamine Release May Involve Activation of Potassium (K+) Channels

subject

description

ABSTRACT Release of oxytocin (Ox) or dopamine (DA) from the isolated neural lobes or neurointermediate lobes, respectively, was evoked by high K + (30 or 45 mM). Naloxone (1-10 μmol/l) which largely enhances the impulse-induced release of Ox had no effect on Ox release evoked by 30 or 45 mM K + . In the presence of 10 mM tetraethylammonium (TEA), Ox release evoked by 30 or 45 mM K + was increased 2-3fold; nevertheless, naloxone caused a further 2-3fold increase. Barium (500 μM) and quinidine (300 μM) antagonized the effect of naloxone observed in the presence of TEA. (-)-Sulpiride (10 μM) enhanced the release of DA evoked by 30 and 45 mM K + by 94 % and 19 %, respectively. TEA enhanced the release of DA evoked by 30 mM K + 2fold and attenuated the effect of (-)-sulpiride by 48 %. These observations suggest that presynaptic opioid receptors, but not DA autoreceptors, may be linked to TEA-insensitive K + channels which are blocked by quinidine or barium.